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Sick Kids researchers confirm that cancer stem cells initiate and grow brain tumours

TORONTO -- Researchers at The Hospital for Sick Children (Sick Kids) and the University of Toronto (U of T) have confirmed that childhood and adult brain tumours originate from cancer stem cells and that these stem cells fuel and maintain tumour growth. This discovery has led to development of a mouse model for human brain tumours and opens the door for new therapeutic targets for the treatment of brain tumours. This research is reported in the November 18, 2004 issue of the scientific journal Nature.

"Now that we have confirmed that a small number of cancer stem cells initiates and maintains human brain tumour growth in a mouse model, we can potentially use the mouse model with each patient's tumour cells to see if therapies are working to conquer that patient's tumour," said Dr. Peter Dirks, the study's principal investigator, a scientist and neurosurgeon at Sick Kids, and an assistant professor of Neurosurgery at U of T. "A functional analysis of the brain tumour stem cell may also give new insight into patient prognosis that may then warrant individual tailoring of therapy."

Dr. Dirks' laboratory was able to regrow an exact replica of patients' brain tumours in a mouse from the isolated cancer stem cells, or brain tumour initiating cells. They were then able to study the growth of the human brain tumour in the mouse model using the advanced imaging technology in the Mouse Imaging Centre (MiCE) at Sick Kids.

Brain tumours are the leading cause of cancer mortality in children and remain difficult to cure despite advances in surgery and drug treatments. In adults, most brain tumours are also among the harshest cancers with formidable resistance to most therapies.

"Next, we are going to study the gene expression of the brain tumour stem cells. Once we have identified what genes are expressed in those cells, we will then be able to target these genes using new drugs or genetic-type therapies," said Dr. Sheila Singh, the paper's
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17-Nov-2004


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